PhD Scientific Days 2024

Poster Session I - Neurosciences 2.

Phenylephrine Produces Alpha 2-mediated Antiallodynic Effect in Rats with Neuropathic Pain

Előadó neve

Abbood, Sarah, PhD

Neptun code

ANGGZ7

Előadó munkahelye

Department of Pharmacology and Pharmacotherapy

Előadó telefonszáma

0036204008873

Előadó e-mail címe

abbood.sarah@phd.semmelweis.hu

Az előadás címe

Phenylephrine Produces Alpha 2-mediated Antiallodynic Effect in Rats with Neuropathic Pain

Szerző(k) neve és munkahelye

Sarah K. Abbood¹, Nariman Essmat¹, Anna R. Galambos¹, Ildikó Miklya¹, Pál Ribal¹, Kornél Király¹, Laszlo G Harsing¹, Mahmoud Al-Khrasani¹

1: Semmelweis University

Bemutatás módja

Poszter

Szekció

Poster Session I - Neurosciences 2.

Language of the presentation

English

Preferred session

Neurosciences

Összefoglaló szövege

Introduction: Neuropathic pain (NP) is a debilitating condition caused by disease or damage of somatosensory neurons. It's treatment remains unsolved fully yet. Finding effective treatment is a clinical challenge because the current treatment approaches have slow onset action and display several side effects. Recently, we have reported that Phenylephrine (PE) displays indirect effect largely due to transporter-mediated norepinephrine (NE) release. Tricyclic antidepressants inhibit the reuptake of NE, which involves in the facilitation of the descending pain pathway. Therefore, we assume that PE might have antiallodynic effect against NP induced by partial sciatic nerve ligation (pSNL).
Aims: To investigate whether intrathecal (i.t.) treatment with PE ameliorates allodynia in rats. In addition, isolated mouse vas deferens (MVD), which hosting both  1 and 2 adrenergic receptors, was applied to assess the receptor profile of PE.
Methods: Male Wistar rats (100-150g) with mono-neuropathy evoked by pSNL were used. NP was indicated by the development of tactile allodynia, namely decrease in the paw withdrawal threshold (PWT) and measured by a dynamic plantar aesthesiometer. The measurement was caried out 2 weeks post operation. Drugs or vehicle were administered in volume of 5µl/rat. First, the antiallodynic effect of i.t. 100, 30, 10 and 3nmole/rat PE was assessed. Next, 30 nmole/rat PE alone or in combination with 10 nmole/rat prazosin or idazoxan was investigated. MVD experiments used male NMRI mice (35–45g) to assess the effect of PE alone or in the presence of prazosin. The antagonist effect of idazoxan was determined against both PE and clonidine.
Results: I.t. PE at dose of 30 nmole/rat showed significant antiallodynic effect peaked at 30min. This effect was retained for PE + prazosin combination but not PE + idazoxan combination. In MVD, prazosin but not idazoxan blocked the postsynaptic effect of PE. On the other hand, idazoxan inhibited 2-mediated clonidine effect.
Conclusion: I.t. PE can acutely ameliorate NP assumedly through spinal 2-mediated action under the present experimental condition. PE might be considered as a new therapeutic option for managing acutely neuropathic patients. To elaborate fully the mechanisms future studies are needed.
Funding: The work supported by Neurology Thematic Programme of Semmelweis Uni-versity (TKP 2021 EGA-25).

University

Semmelweis University

Supervisor

Mahmoud Al-Khrasani

Publication of my abstract

I do not give consent to the publication of my abstract on the website of the congress.

Kind

Szabad

Status

elfogadva

Accepted presentation method

poszter

Előadás fájl jóváhagyás

nem rendelkezett róla

Előadó

8085

Start

14:55

End

14:58